Thursday, 21 August 2003
This presentation is part of : Thursday Poster Sessions

PD-016 The Effect of Bright Light Therapy on the Sleep-Wake Rhythm in Institutionalized Patients with Alzheimer’s Disease

Glenna A. Dowling1, Erin M. Hubbard2, Judy Mastick2, Jay S. Luxenberg3, Eus J. W. Van Someren4, and Shirley Wu5. (1) University of California, San Francisco, San Francisco, CA, USA, (2) Institute on Aging, San Francisco, CA, USA, (3) Jewish Home, San Francisco, CA, USA, (4) Netherlands Institute for Brain Research, Amsterdam, Netherlands, (5) IOA, San Francisco, CA, USA

Objective: The purpose of this study was to test the effect of bright light therapy on sleep-wake (circadian) rhythm in patients with AD.

Design: In this double-blind randomized clinical trial, subjects were assigned to experimental (bright light) or control groups.

Materials and Methods: 50 subjects completed the protocol (mean age 86+8). The experimental group received 1 hour (0930-1030) of bright light exposure (2500 lux in gaze direction) daily for 10 weeks, the control group received usual indoor light (~150-200 lux). Sleep-wake data were obtained using wrist actigraphy for 1 week at baseline and week 10 of the intervention. Circadian rhythm parameters were assessed using nonparametric techniques:

a) interdaily stability (IS) - quantifies the degree of resemblance between activity patterns of individual days, theoretical range of 0-1, higher values indicate a more stable rhythm;

b) intradaily variability (IV) - quantifies the fragmentation of periods of rest and activity, theoretical range 0-2, higher values indicate a more fragmented rhythm;

c) relative amplitude (RA) - reflects the normalized difference between the most active 10-hour period and the least active 5-hour period in an average 24-hour pattern, theoretical range from 0-1, higher values indicate a stronger rhythm; and

d) L5 – sequence of the 5 least active hours, average activity during L5 provides an indication of regularity and restfulness of sleep periods, lower values indicate more restful sleep.

T-tests were used to compare mean change scores (baseline – end of intervention) for experimental and control groups.

Results: Nonparametric circadian analyses revealed no significant difference between groups on IS, IV, RA, or L5. However, there was a wide variability in L5 onset at baseline. Given the usual institutional bedtime of 2000 and rise time of 0800, we categorized subjects into 2 groups based on L5 onset. Non-aberrant onset times were defined as those between 20:00 and 03:00 and aberrant times between 03:01 and 19:59. Using this definition, 16 subjects were aberrant (n=10 experimental, n=6 control) and 34 subjects were non-aberrant (n=23 experimental, n=11 control). Subjects with aberrant rhythms in the experimental group exhibited a significant increase in RA (t=-2.4, p<.04) and decrease in L5 (t=2.5, p<.03). There were no other significant differences.

Conclusions: While group data analyses revealed no significant differences between experimental and control groups, rhythm amplitude and L5 improved in experimental subjects who had aberrant rhythms at baseline. Subsequent analyses will focus on determining each subjects’ endogenous time vis-ŕ-vis the timing of the light to examine whether light was administered during the sensitive period of the phase response curve and establish a dose-response curve.

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